The Impact of Development and Sensory Deprivation on Dendritic Protrusions in the Mouse Barrel Cortex

Abstract

Dendritic protrusions (spines and filopodia) are structural indicators of synapses that have been linked to neuronal learning and memory through their morphological alterations induced by development and experienced-dependent activities. Although previous studies have demonstrated that depriving sensory experience leads to structural changes in neocortical organization, the more subtle effects on dendritic protrusions remain unclear, mostly due to focus on only one specific cell type and/or age of manipulation. Here, we show that sensory deprivation induced by whisker trimming influences the dendritic protrusions of basilar dendrites located in thalamocortical recipient lamina (IV and VI) of the mouse barrel cortex in a layer-specific manner. Following 1 month of whisker trimming after birth, the density of dendritic protrusions increased in layer IV, but decreased in layer VI. Whisker regrowth for 1 month returned protrusion densities to comparable level of age-matched controls in layer VI, but not in layer IV. In adults, chronic sensory deprivation led to an increase in protrusion densities in layer IV, but not in layer VI. In addition, chronic pharmacological blockade of N-methyl-d-aspartate receptors (NMDARs) increased protrusion density in both layers IV and VI, which returned to the control level after 1 month of drug withdrawal. Our data reveal that different cortical layers respond to chronic sensory deprivation in different ways, with more pronounced effects during developmental critical periods than adulthood. We also show that chronically blocking NMDARs activity during developmental critical period also influences the protrusion density and morphology in the cerebral cortex.

Development and sensory experience dependent regulation of microglia in barrel cortex

“…Furthermore, microglia have been implicated in synaptic remodeling during development through synaptic stripping (Z. Chen et al, ; Trapp et al, ; Tremblay et al, ) and induction of dendritic spines (Miyamoto et al, ). Given the fact that prolonged trimming leads to abnormality of dendritic spines (a proxy of excitatory synapses) in the barrel cortex (Chen, Bajnath, & Brumberg, ), coinciding with our current observation of increased activation of microglia, it is possible that activated microglia play a role in the alterations of synaptic structures within neocortical circuitry during developmentally critical periods (Michell‐Robinson et al, ; Miyamoto et al, ; Rochefort et al, ; Tremblay & Majewska, ; Ueno & Yamashita, ).…”

“…Past studies have extensively characterized the effect of chronic sensory deprivation on neuronal morphology (Chen, Bajnath, & Brumberg, ; C.‐C. Chen et al, ), physiology (Lee, Land, & Simons, ; Simons & Land, ) and whisker‐related behavior (Carvell & Simons, ) in the barrel cortex.…”

“…Table details the total number of animals in each experimental group. Developmental ages were picked based on previous studies in the laboratory allowing for direct comparisons (Chen et al, ; Chen, Bajnath, & Brumberg, ; Chen, Chu, & Brumberg, ; McRae et al, ).…”

Oxytocin is implicated in social memory deficits induced by early sensory deprivation in mice

“…The alterations in the brain caused by the early sensory deprivation are not limited to loss of barrels. For example, the early sensory deprivation also affects synaptic plasticity [14, 15], dendritic spine refinement and formation of local circuitry [16–20], and inter-hemispheric in the somatosensory cortex [22]. We thus speculated the spatial memory and social memory deficits in ION-transected mice are the consequence of global structural and functional alterations in brain circuits after the early sensory deprivation.…”

“…In addition, plasticity of cortical neurons are also changed after sensory deprivation, for example layer IV neurons rapidly diminishes synaptic plasticity after sensory deprivation [14, 15]. Sensory experience also affects dendritic protrusions and local circuitry [16–20] suggesting possible implication in the process of learning and memory.…”